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The appearance of a swine type of influenza A among recruits in Fort Dix, New Jersey, in 1976 prompted an evaluation of the sensitivity of this virus to amantadine - HCl. Well-tolerated levels of the drug effectively blocked replication of the influenza A/New Jersey/8/76 (Hsw1N1) virus isolate in three laboratory models: monkey kidney cells, embryonated eggs, and intranasally infected mice. On a comparative basis this virus would appear to be more sensitive to amantadine - HCl than human influenza A strains, including the recent Victoria (1975) strain. All strains of influenza A virus continue to be sensitive to amantadine - HCl.

I-Adamantanamine (amantadine) causes a selective, reproducible, dose-related inhibition of influenza infections in tissue culture, chick embryos, and mice. The compound is not virucidal and appears to act by interfering with the penetration of the host cell by the virus. In influenza infections of mice, greatest efficacy occurs with treatment at the time of infection; however, there is significant antiviral activity with treatment delayed up to 72 hours after infection. Virus inhibition is not complete and survivors are immune to a challenge infection with the original infecting virus.